1. Field of the Invention
The present disclosure relates to methods for treating spinal cord injury.
2. Description of Related Art
Spinal cord injury (SCI) refers to damage to the spinal cord resulting from trauma (e.g. a car crash) or from disease (e.g. cancer) or degeneration. According to WHO statistics, as many as 500,000 people suffer a spinal cord injury every year, with road traffic crashes, falls and violence as the three leading causes.
SCI causes loss of neurons and axons resulting in motor and sensory function impairments. For adult mammals, SCI may cause incurable neurological dysfunction due to failure of axonal regeneration. Symptoms of SCI depend on the severity of injury and its location on the spinal cord; common symptoms include partial or complete loss of sensory function or motor control of arms, legs, and/or body, while the most severe SCI may affect the autonomic systems that regulate breathing, bowel and bladder control, heart rate, and blood pressure. Most people with SCI experience chronic pain, and an estimated 20-30% of SCI patients exhibit clinically signs of depression, which in turn has a negative impact on improvements in functioning and overall health of the patient. Also, SCI may render a person dependent on caregivers. Accordingly, spinal cord injury may result in devastating psychological and psychological damage to the affected individuals and cause an enormous financial cost to the patients and/or their families.
The pathophysiological processes that underlie SCI comprise multiple phases of injury. Initial physical trauma to the spinal cord contains traction injury, compression forces, and direct mechanical disruption of neural elements. Microvascular injuries with hemorrhage and disruption of blood-spinal cord barrier are followed by edema, ischemia, release of cytotoxic chemicals from inflammatory pathways, and electrolyte shifts. Subsequently, the secondary injury cascade is ignited that compounds the initial mechanical injury with cell necrosis and apoptosis to endanger surviving neurons in the neighborhood. Progression from the acute to the chronic phase results in secondary neurodegenerative events, such as demyelination, Wallerian degeneration, and axonal dieback, while a non-permissive tissue environment is established largely because of astroglial scar formation, thus contributing to irreversible loss of function. The inflammatory response plays a critical role in the secondary phase after SCI through modulation of a series of complex cellular and molecular interactions, which further reduce the chance of recovery of penumbra neurons and render functional recovery almost hopeless.
In spite of decades of research and development, the cure for severe SCI remains elusive and current treatment is limited to early administration of high dose steroids and acute surgical intervention to minimize cord edema and the following cascades of injuries. Accordingly, there exists a need in the art for providing for treating spinal cord injury or to improve the locomotor function recovery of a spinal cord injured subject.